ARDS is a syndrome in which closed alveoli do not perform oxygenation while blood flow still perfuse the capillaries surrounding the closed alveoli. This leads to a low ventilation/perfusion ratio (VA/Q) and severe hypoxia. However, upon early ARDS, there is no respiratory pump failure: the disease is restricted to oxygenation not to elimination of CO2.
Patients diagnosed with acute respiratory distress syndrome (“ARDS”), are typically treated with controlled mechanical ventilation (CMV) and conventional sedation (typically benzodiazepine-opiate: usually midazolam-sufentanil) and, optionally, a muscle relaxant. Upon refractory hypoxia, adjunctive therapy may be required: prone positioning, NO, sildenafil, almitrine, etc. . . . . Most patients do not die from refractory hypoxia but from pre-existing co-morbidities or complications arising from prolonged stay in the critical care unit (CCU): sepsis, cardiac failure, multiple organ failure (MOF). Therefore, contrary to the views expressed by authorities (1), treatment of ARDS is to shorten the length of intubation (i.e. “fast-tracking” extubation), stay in the CCU and reduce the incidence of iatrogenic complications.
The core progress over the last 10 years was the combination of a few physiological and epidemiological studies, to avoid barotrauma and volutrauma: a) use of a Pplat (maximal pressure measured upon end-inspiration)≦26-32 cm H2O b) use of low tidal volumeVt≦5-6 ml·kg-1 of body weight (BW) compatible with such a low Pplat. However, the cornerstone of the treatment still relies on CMV (or related modes of ventilation: assist control, IMV, etc.) at variance with maintenance of spontaneous ventilation. Worse, some advocate the use of an early 48 h course of myorelaxation (2). Most commentators have skipped the fact that this group switches his patients over to spontaneous ventilation-pressure support (SV-PS) after this 48 h course (2, 3).
Few groups advocate the use of spontaneous ventilation (SV) upon ARDS (4-6), without a clear-cut schema for this use. Moreover, experienced investigators advocate against the use of SV upon early severe ARDS, when oxygen demands are high (7). The only group which provides such a clear-cut schema, uses a combination of midazolam and opiates which a) depresses the ventilator drive, at variance with the use of SV b) generates an elimination process which appears at odd with the objective of fast tracking the extubation. The article which describes this known method is: “Putensen C, Zech S, Wrigge H, Zinserling J, Stuber F, von S T, et al. Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Respir Crit Care Med. 2001; 164(1): 43-9” (5).